Data from several animal models as well as human studies have demonstrated that in utero exposure to maternal hyperglycemia results in fetal B cell hyperplasia, hyperinsulinemia, and subsequent predisposition to obesity and glucose intolerance. However, it is uncertain whether the premature B cell hyperstimulation is itself critical to lifelong glucoregulatory disturbances, or whether the effects of fetal hyperinsulinism on target tissues is essential in precipitating subsequent obesity and glucose intolerance. We propose to delineate the individual..